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. 2015 Oct 1;8(10):1237–1246. doi: 10.1242/dmm.021071

Fig. 5.

Fig. 5.

C4PY exerts inhibitory effects through GPER in CAFs. (A) ERK1/2 and Akt activation in CAFs treated for 5 min with 1 nM E2 and 100 nM G-1 is prevented by 1 µM C4PY. (B) Densitometric analysis of the blots normalized to ERK2 and Akt, respectively. Each data point represents the mean±s.d. of three independent experiments. (C) The mRNA expression of CTGF and Cyr61 induced in CAFs by 1 h treatment with 1 nM E2 and 100 nM G-1 is prevented by 1 µM C4PY, as evaluated by real-time PCR. Results obtained from experiments performed in triplicate were normalized for 18S expression and shown as fold change of RNA expression compared to cells treated with vehicle. Each data point represents the mean±s.d. of three independent experiments performed in triplicate. (D) CTGF and Cyr61 protein expression induced in CAFs by 2 h treatment with 1 nM E2 and 100 nM G-1 is inhibited in the presence of 1 µM C4PY. (E) Densitometric analyses of the blots normalized to β-actin; values shown represent the mean±s.d. of three independent experiments. (F) The migration of CAFs upon treatment with 1 nM E2 and 100 nM G-1 is inhibited by 1 µM C4PY, as evaluated by Boyden Chamber assay. Each data point is the average ±s.d. of three independent experiments performed in triplicate. (•) and (◦) indicate P<0.05 for cells receiving vehicle (–) versus treatments.